HSP90AB1 (Heat Shock Protein 90 Alpha Family Class B Member 1)

Additionally, HSP90B1 might enhance glioma metastasis and resistance to radiotherapy by regulating RhoC expression. This regulatory effect was achieved by the directly binding of HSP90B1 to RhoC, thereby preventing its degradation through the ubiquitin-proteasome pathway.

Finally, through virtual screening and Co-IP, we identified ivermectin as a potent inhibitor of the HSP90AB1-ITGBL1 interaction, and treatment with ivermectin dramatically inhibited OS progression in vivo. In conclusion, we uncover a novel mechanism that promotes OS progression and identify a new candidate drug for the treatment of OS.

Crucially, the HSP90AB1 K265R mutation or pharmacological inhibition of ACOX1 (10,12-tricosadiynoic acid) or TXN (1-methyl-propyl 2-imidazolyl disulfide, PX-12) synergizes with cisplatin to suppress tumor growth in vivo by disrupting redox adaptation. These findings reveal that crotonylation is a hypoxia-sensitive rheostat for TXN-mediated redox control, suggesting that the ACOX1-HSP90AB1-TXN axis is a therapeutic vulnerability in therapy-resistant OSCC.

Subsequent SHAP analysis revealed SRC, HSP90AB1, HSP90AA1 and CDK1 as the key contributors to prognostic prediction, with each being highly expressed in BC and linked to poor clinical prognosis. Notably, among all chemicals screened, Disperse Yellow 3 exhibited the strongest binding affinity to these four key targets, demonstrating the strongest association with BC risk.

Diff-Metabolic cells retained liver-specific functions with favorable prognosis, whereas the other three programs correlated with disease advancement; notably, all four states exhibited differential therapeutic vulnerabilities, including sorafenib resistance...Geneformer-based virtual knockout screening identified HSP90B1 as a convergent dependency, validated by its cancer cell essentiality, HCC overexpression, abundance in treatment-resistant tumors, and association with adverse survival. This integrated atlas establishes a framework for targeting tumor-intrinsic states and microenvironmental dependencies in HCC.

SB may regulate TRP-induced bone metabolism abnormalities in LNCaP cells through the IL-17 signaling pathway as well as five DEPs: p-ERK2, RELA, HSP90B1, GNAI1and GNAI3.

Consistently, down-regulation of CYP1A2 and CYP2C9 and up-regulation of HSP90AB1 were shown by immunofluorescence/Western blotting/RT-qPCR, impairing signaling networks and immune homeostasis and ultimately leading to the establishment of hepatotoxicity and carcinogenic microenvironments. Collectively, the TCDD "target binding-pathway dysregulation-immune imbalance-pathological damage" cascade has been systematically delineated, providing novel targets and a theoretical framework for therapeutic intervention against pollutant-associated liver diseases.

This study presents a promising non-invasive biomarker panel for oral and oropharyngeal SCC detection. Further validation in larger cohorts is needed to confirm diagnostic value and clarify sex specificity. The approach is adaptable to other tumour types and sample materials, supporting molecular diagnostics. The workflow shows all project steps from sampling to marker localisation in FFPE tissue. In the discovery phase, RNA sequencing was used to find potential mRNA markers in swab samples. Via strict filtering, markers for RT-qPCR were selected and verified in a bigger cohort in the validation phase. Selected markers were then used to do combinatorial analysis to improve the specificity and sensitivity compared to that of the single markers. Finally, markers were verified and localised in primary oral and oropharyngeal SCC FFPE tissue. Created with BioRender.com.

Based on analyses of public databases and computational predictions, DHA may exert anti-HCC effects by regulating the p53 signaling pathway, cell cycle progression, and the LMRGs. However, these potential regulatory mechanisms require further experimental validation to confirm their biological relevance.

This integrative multi-omics analysis provides compelling evidence that BPA may facilitate ESCA progression through HSP90AA1/HSP90AB1-mediated oncogenic and immune-inflammatory pathways. These findings deepen understanding of environmental carcinogenesis and suggest potential molecular targets for ESCA prevention and treatment.

Forced overexpression of HSP90AB1 enhanced BCa development in vivo, which was mitigated by MSAB. In conclusion, our findings suggest that ALT exerts anti-cancer activity in BCa, potentially through modulation of HSP90AB1 and β-catenin signaling pathways.

The results of in vitro cell culture experiments showed that a specific thiazolone derivative had a significant inhibitory effect on RD cell lines, providing a scientific basis for the discovery of new targets and effective compounds for the treatment of RD. This study revealed the mechanisms of thiazolone derivatives in the treatment of RD through a combination of network pharmacology and in vitro experiments and provided a new perspective for future drug development and treatment strategies.